Citations

A case is reported of a 20-day-old infant with origin of the right pulmonary artery from the ascending aorta. Besides its abnormal origin, the artery was stenotic in its proximal half. We believe the malformation results from persistence of the distal (instead of the proximal) part of the primitive sixth aortic arch and of a portion of the right dorsal aorta. The presence of ductal tissue in the wall of the right pulmonary artery supports this concept. The pulmonary vasculature in the two lungs showed great differences in medial and intimal characteristics. A second case of origin of the right pulmonary artery from the aorta, deseribed elsewhere, provided material for comparative study of the structure of the right main pulmonary arteries and the intrapulmonary branches.

The present study presents pertinent clinical and pathologic findings in 20 cases of ruptured mitral chordae tendineae encountered at the Mayo Clinic between 1934 and 1958 inclusive. Mitral insufficiency results from the rupture of chordae tendineae, the severity being related to the number of chordae ruptured. The resulting heart disease may be severe and may progress to cardiac decompensation and death. Bacterial endocarditis was the major etiologic factor in rupture of the chordae tendineae in this study.

An anatomicopathologic entity of the tetralogy of Fallot with an additional finding of an accessory flap of tricuspid valvular tissue is described. In the 3 cases reported in this paper, the outstanding hemodynamic finding was a right ventricular systolic pressure that was significantly greater than the systemic systolic pressure. The hemodynamic findings were explained by the fact that the accessory tricuspid flap partially closed the large ventricular septal defect. The clinical picture was similar to that of either severe pulmonary stenosis with an intact ventricular septum or severe pulmonary stenosis with a small ventricular septal defect and a right-to-left shunt at the ventricular level.

In a pathologic collection of 722 congenital heart lesions we have observed 10 cases in which a ventricular septal defect was associated with obstruction to normal left ventricular outflow. These cases are presented in the framework of a classification relating hemodynamics to the position of the obstructing lesion and the size of the ventricular septal defect. One additional case observed clinically and at operation is also reported to make more nearly complete the classification of the anatomic arrangements in which the common denominators are ventricular septal defect and obstruction to normal ventricular outflow.

A study was made of the configuration of the elastic tissue of the pulmonary trunk in 6 cases of idiopathic pulmonary hypertension. The ages of the patients ranged from 12 to 54 years. The pattern was that of the adult pulmonary type in the 5 female patients, whereas it more closely resembled the fetal, aorta-like type in the single male patient. These data are interpreted as indicating that idiopathic pulmonary hypertension is acquired in most cases but that it may be present from birth in a minority of instances.

This study attempts to bring into focus certain details which have not been described adequately in textbooks of anatomy. This information is now of considerable significance because of its role in the genesis and surgical treatment of mitral stenosis. Variations in the size and shape of the mitral valve are described, with particular reference to the fact that valve commissures, or junctional zones between the leaflets, occur in the normal valve. Measurements of commissures, chordae tendineae and valve leaflets are presented, with a discussion of the significance of some of these measurements.

The purpose of this investigation was to study the incidence and location of systemic arterial occlusion and pulmonary embolism in a consecutive series of cases of fatal acute myocardial infarction. Another consecutive series of cases in which healed myocardial infarction was demonstrated at necropsy was similarly studied. In none of the cases included in this study had anticoagulant therapy been employed. Massive pulmonary embolism was the most frequent fatal thrombo-embolic complication found among the cases of acute myocardial infarction. Cerebral infarction was the most frequent fatal thrombo-embolic complication found among the cases of healed myocardial infarction. Cerebral infarction was the most frequent fatal systemic arterial thrombo-embolic lesion in both groups. Acute splenic and renal infarcts were frequently demonstrated but with one exception appeared to play an incidental role in the clinical course of the patients. Although systemic arterial occlusion was frequently found in association with intracardiac mural thrombi, there were many other cases in which evidence of systemic arterial occlusion was found in the absence of intracardiac mural thrombi. A positive correlation existed between the presence of pulmonary and systemic arterial occlusion and the occurrence of congestive cardiac failure.

This is a study of the location and incidence of intracardiac thrombi in acute and in healed myocardial infarction. In myocardial infarction intracardiac thrombi occur predominantly in the left ventricle. Anterior myocardial infarcts are more commonly associated with mural thrombi than posterior myocardial infarcts. Large myocardial infarcts and congestive failure are factors which predispose to the formation of left ventricular mural thrombi in myocardial infarction.